Victoria Luu
1235186
BME 80H – Human Genetics Research Paper
The Mutation of the p53 Gene and Its Impact on Lung Cancer
Cancer occurs when new cells are born to replace old cells but the old cells do not undergo apoptosis, as they normally should. Instead, the new cells come together to form tumors that can potentially become malignant, meaning they have the ability to chew through the basal lamina and enter the bloodstream to spread to new environments throughout the body. Cancer could also occur due to cell overproliferation because what normally controls the cell cycle and keeps cell division in check has either been mutated or been deleted (Dugdale, 2012). p53 is a tumor suppressor gene that prevents the cell cycle from advancing past the restriction point at the end of G1 phase when DNA damage is detected so that DNA damage repair machinery has time to fix the damage before the cell is able to proceed to S phase. If the damage is beyond repair, p53 sends the cell down the apoptotic pathway instead (Kimball, 2013). The main purpose of p53 is to maintain the balance between cell proliferation and apoptosis, but without p53, there will be a greater number of cells with DNA damage that neither get repaired nor killed. Genomic mutations arise and build-up as a result, and the chance of tumor formation increases (Mendoza-Rodriguez and Cerbón, 2001).
The tumor suppressor gene p53 plays an extremely important role in the cell cycle and for maintaining a tumor-free system overall. So it is not surprising that p53 mutations are found to be connected to many different types of cancer (Johnson, 2013). Such p53 mutations give rise to mutant p53 proteins, which have lost its normal function of suppressing tumor formation and have ga...
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...esearchers have looked into would be the promotion of ubiquitination of the mutant p53 genes, which would signal for its degradation through the proteasome (Muller, 2014). While the strategies sound simple enough to follow through, their success depends their efficiency in targeting mutant p53 genes in cancer treatments, their potential side effects on other genes and pathways, and their ability to actually target the correct cells containing the tumor suppressor gene mutation.
While there have been many ideas to treat p53 mutations, most have not been tested in clinical trials because of the complexity of the human body and its cellular pathways, which researchers and scientists must further follow up on and understand in order to finally put their therapeutic strategies into practice later down the road in treating cancers with p53 mutations.
Wang, Chih-Hung, et al. "Simian Virus 40 T Antigen Induces p53-Independent Apoptosis but does Not Suppress erbB2/neu Gene Expression in Immortalized Human Epithelial Cells." Cancer letters 137.1 (1999): 107-15.
Specifically “TP53, p16INK4A, and SMAD4. The p53 nuclear protein activates transcription of a cyclin kinase inhibitor p21WAF1/CIP1. Following genomic stress, inappropriate growth factor stimulation or expression of oncogenic ras increased expression of p53, and thus p21WAF1/CIP1 resulted in inactivation of specific CDK/cyclin complexes” (MedScape). If this transformed cell can escape internal and external fail-safe mechanisms, receive nutrients, and activate its proliferative program, it can form a mass of cancerous cells. Tumor growth can cause the loss of pancreatic functions. Another characteristic of pancreatic cancer is metastasis happens early in tumor growth, which is most likely responsible for pancreatic cancer’s aggressive
Cancer is the term used to describe a group of diseases consisting of hundreds of ailments and although there exists so many different types of cancer, they all begin in a similar way. The body is made up of over a trillion cells, and cancer is the uncontrolled growth of malfunctioning cells in the body (Dawson, 1996). “Normal body cells grow, divide, and die in an orderly fashion. During the early years of a person’s life, normal cells divide faster to allow the person to grow. After the person becomes an adult, most cells divide only to replace worn-out or dying cells or to repair injuries” (American Cancer Society, 2012).
Chemoprevention requires treatments that are administered to presumably healthy, asymptomatic subjects who do not have cancer, but do have risk factors associated with an increased probability to cultivate the cancer which the experimental intervention is theorized to condense. So, chemoprevention research involves at-risk research subjects who are neither patients diagnosed with disease, as in treatment trials, or typical healthy volunteers. There is a growing interest and investment in research on cancer chemoprevention. Several major cancer chemoprevention trials have been conducted in the United States, including trials testing the effectiveness of tamoxifen, both alone and later compared to raloxitene, to prevent primary invasive breast cancer; finasteride to prevent prostate cancer; and beta-carotene to prevent lung cancer.
...y may be another area of research that may enhance anti-tumor activity. Creating better antibodies, like rituximab and others we are able to better target the tumor cell. There are many targets on our bodies immune cells and by being able to locate them specifically and boost the immune system in order for it to work better than it already can proves to be beneficial and harnessing this power can lead to a dramatic impact on the way we treat cancer. Maintaining and preserving patients quality of life and looking for lifelong cure is what scientists are looking for. Improving the efficacy of these immunotherapy treatments can lead to significant breakthroughs including longterm remission and being able to treat patients with cancer that is hard to treat. I look forward and can't wait to see the advances that will be made in this field or research in the near future.
Thought to be an oncogene, a gene that has potential in transforming normal cells into tumor cells, p53 was regarded as the most prominent tumor suppressor gene [1]. P53 is a gene which signals apoptosis (programmed cell death) if a cell cannot be repaired due to an extensive amount of damage. As stated in the textbook, p53 regulation occurs by an E3 ubiquitin-protein ligase known as MDM2 [1]. "Controlling the controller" is a statement that describes the molecular interaction where the presence of MDM2 targets the p53 for proteosome via degradation. With three main checkpoints in cell cycle, the literature states p53 functioning from G1 into S phase in a chaotic cell [2]. The normal state of cells is to keep p53 levels low in order to prevent uncontrolled apoptosis and random cell cycle arrest from occurring. In a further note, although p53 promotes apoptosis and cell cycle arrest, cancer may result from p53 unable to recognize the problematic site. In turn, a mutation in p53 may result engaging in new activities. These activities include cellular transformation, tumor metastasis,...
Cancer starts when cells in a part of the body start to grow out of control. Cancer cell growth is different from normal cell growth. Instead of dying, cancer cells continue to grow and form new, abnormal cells. Cancer cells can also invade (grow into) other tissues, something that normal cells cannot do. Growing out of control and invading other tissues are what makes a cell a cancer cell. Cells become cancer cells because of DNA (deoxyribonucleic acid) damage. DNA is in every cell and it directs all the cell’s actions. In a normal cell, when DNA gets damaged the cell either repairs the damage or the cell dies. In cancer cells, the damaged DNA is not repaired, and the cell doesn’t die like it should. Instead, the cell goes on making new cells that the body doesn’t need. These new cells all have the same abnormal DNA as the first cell does.
Diagnosed with lung cancer, now what!? Time to do some research. Lung cancer is the number one cause of deaths in males and females. The causes, diagnosis, and treatment of lung cancer have advanced recently with new technology available to scientists and the medical profession. Lung cancer develops when the cells grow abnormally and tumors form instead of healthy lung tissue. It can take place in one or both lungs, normally the cells that line the air passages. Not all tumors are cancerous, the ones that do not spread are benign tumors. The more tumors that develop in the lungs will cause the lungs to work less efficiently. The metastatic tumors spread to other parts of the body passing through the blood stream or lymphatic system.
Tumors are formed by the alteration of the body’s own cells. This can be caused by environmental factors such as radiation, like UV exposure, chemicals or viruses 1. These can disrupt genes that control growth and cause an increase in cell division and proliferation. Proto-oncogenes are those genes that control normal but essential cell processes that keep cell growth and death in check. Two important categories are apoptosis genes, which regulate cell death, and tumor suppressor genes, which decrease cell propagation 1 . If these genes were mutated to the point where they cannot produce a functioning protein, cell division would continue far past what it was supposed to and unhealthy cells would be allowed to live and continue to multiply. This is what creates a malignant tumor. Certain conditions in the body can also promote the growth of cancer cells. One of these is a deficiency of natural killer (NK) cells, which are able to kill cancer cells by creating a pore in the cell membrane with perforin and releasing granzymes into the cell. Low levels of perforin allow for tumor growth 1. Chronic inflammation can also ...
Healthy cells grow and divide in a way to keep your body functioning properly. But when a cell is damaged and becomes cancerous, cells continue to divide, even when new cells aren't...
Usually, normal cells die when they are old or damaged, newly grow cells will replace them. However, if something goes wrong, there may be too many new cells when the body only needs a few of them, and the body can’t get rid of old cells, it builds up a mass of tissue called tumor. There are two types of tumor, begin or malignant. Begin tumors are usually not harmful to human body, however, malignant tumors could be life threatening. This type of tumors will invade organs and tissues around them, travel through blood vessels or lymph vessels, attach to other tissues and destroy them. Malignant tumors arise in breast tissues and cause breast cancer.
Mutations turn genes on and off, activating diseases; all women have a chance of developing breast cancer (Understanding; Breast). Unhealthy cells divide and form a tumor. The tumor can be benign and not dangerous. Malignant tumors can become potentially dangerous (Understanding). The cancer becomes invasive when it spreads to other breast areas. Cancer that has not invaded other breast tissues remains noninvasive; noninvasive cancer can become invasive if not treated (Chen, 2010). If cancer cells get into the lymph nodes, the cells can get into the bloodstream and spread throughout the body (Understanding; Rosen, 2011).
The American Cancer Society publishes current advances made in cancer research on their website. Many of the exciting discoveries about how best to treat the disease focus on the genetic aspects associated with certain types of cancer. In addition, treatments aimed at genetic solutions to cancer may be more effective and may cause fewer adverse side effects than traditional cancer treatments (American Can...
Cancer develops when cells in a part of the body begin to grow out of
Cancer is a disease that affects human somatic cells. It causes the cells to divide uncontrollably and form masses known as tumors. There are two different types of cancer tumors. Some tumors are benign and other tumors are malignant. Benign tumors look similar to the tissues that they came from and develop slowly. The tumor remains in the same area that the tumor originated in. Malignant tumors are formed from cells that do not resemble the tissue that they came from. They vary in shape and size. This enables pieces of the tumor to break off and spread to other places in the body. Over the past few decades cancer has become a very prominent disease. There are many different types of cancer and many different causes for the the disease. Most cancers are because of a genetic mutation. The most common type occur when a cell is dividing. Proto-oncogenes, which are alleles in a normal cells, mutate to form oncogenes. These oncogenes cause cancer because they do not allow the cells to self destruct or become epistatic. There have been several research projects which have been testing epistatis.